Basic experimental studies have confirmed that the potential mechanisms of renal injury due to hyperuricemia induce inflammation, afferent arteriopathy [16], and endothelial dysfunction [18]; activate the renin-angiotensin-aldosterone system (RAAS) [17] and cyclooxygenase-2 (COX-2) expression; and impair oxidative metabolism [12], among others. Here, PTGS2 is linked to endothelial dysfunction.